Psychophysical investigation of second-order spatial vision in amblyopia

Purpose. Amblyopia has recently been shown to result in deficits in detection of contrast defined (second-order) patterns, which are widely believed to be processed predominantly in early extrastriate cortex (V2). These 5 studies investigate whether this deficit is associated with (1) amplification of the loss for first-order input, (2) an abnormal non-linearity to luminance (first-order input), (3) abnormal second-order lateral interactions, (4) spatial summation, and (5) contrast discrimination.; Methods. We used stationary modulations of contrast and psychophysically determined thresholds for contrast detection and contrast discrimination. We extensively tested groups of amblyopic, non-binocular/non-amblyopic, and normal adult observers. Amblyopic and fellow non-amblyopic eyes were compared to normal eyes because non-amblyopic eyes are known to show second-order deficits.; Results. (1) Relative to 4 controls, 5 of 6 amblyopic eyes and 3 of 6 non-amblyopic eyes showed reduced second-order contrast sensitivity (roughly a factor of 2). The loss was greater than the loss for first-order spatial input. (2) 6 controls and each eye of 6 amblyopes showed similar perception of sinusoidal changes in luminance, indicating an essentially equal non-linear transformation of luminance. (3) In 5 controls, second-order contrast detection was facilitated (average 12%) by spatially isolated, collinear and orthogonal second-order flanks. The flanks suppressed detection (up to 45%) in each eye of 7 of 8 non-control observers. (4) 4 controls and each eye of 8 non-controls showed essentially equal second-order spatial summation. Summation ended at ∼8 cycles and was independent of second-order contrast sensitivity. (5) 5 controls showed dipper functions (increment thresholds 0.4–0.7× pedestal contrast threshold (PCT)). In 8 non-control observers, 2 of 6 amblyopic eyes (the two deepest amblyopes) showed shallow dippers (increment thresholds 0–.4× PCT). The remaining eyes showed equal or smaller increment thresholds than controls.; Conclusions. Amblyopic and fellow non-amblyopic eyes as well as non-amblyopic observers lacking binocular vision show larger deficits in second-order contrast detection than discrimination, and abnormal lateral interactions but normal summation of spatial channels. These abnormalities may reflect inhibition of normal populations of second-order neurons. Amblyopia appears to result in propagation and amplification of neural deficits from V1 to early extrastriate cortex (V2).